Background: Recently, long non-coding RNAs (lncRNAs) have been elucidated to play essential roles in cancers, and the recognition of lncRNA expression patterns in nasopharyngeal carcinoma (NPC) may be helpful for indicating novel mechanisms underlying NPC carcinogenesis. Herein, we conducted this study to probe into the function of lncRNA ZNF667-AS1  in NPC progression with the involvement of microRNA-1290  (miR-1290 ) and actin-binding LIM protein 1 (ABLIM1 ).
Materials and Methods: In silico analysis screened differentially expressed genes and miRNAs in NPC and predicted potential mechanisms. ZNF667-AS1  expression was detected in NPC tissues and cells. The gain-and-loss function assays were performed to explore the effects of lncRNA ZNF667-AS1 and miR-1290  in NPC cell biological behaviors. In vivo experiments were further conducted to confirm the in vitro results.
Results: In silico analysis predicted that ZNF667-AS1  was diminished in NPC, which may downregulate ABLIM1  through sponging miR-1290 . ZNF667-AS1  was poorly expressed in NPC tissues and cells, and overexpression of ZNF667-AS1  inhibited growth of NPC cells. ZNF667-AS1  competitively bound with miR-1290 , thereby upregulating ABLIM1 . miR-1290  resulted in the promotion of NPC cell progression by suppressing ABLIM1 . Overexpression of ZNF667-AS1  or suppression of miR-1290  inhibited tumorigenicity of NPC cells in vivo.
Conclusion: This study highlights that lncRNA ZNF667-AS1  promotes ABLIM1  expression by sponging miR-1290  to suppress NPC cell progression.
Keywords: nasopharyngeal carcinoma, lncRNA ZNF667-AS1 , ABLIM1 , microRNA-1290 , competing endogenous RNA